U.S. patent number 5,989,267 [Application Number 08/893,856] was granted by the patent office on 1999-11-23 for method of hair removal.
This patent grant is currently assigned to The General Hospital Corporation. Invention is credited to Richard Rox Anderson.
United States Patent |
5,989,267 |
Anderson |
November 23, 1999 |
Method of hair removal
Abstract
The invention features a method of removing a hair, involving
mechanically or chemically removing the hair to expose the follicle
of the hair, and then treating the follicle to inhibit its ability
to regenerate a hair. Removing the hair facilitates the uptake of a
follicle-inactivating compound and thus allows for long-term
inhibition of hair growth.
Inventors: |
Anderson; Richard Rox
(Lexington, MA) |
Assignee: |
The General Hospital
Corporation (Boston, MA)
|
Family
ID: |
23218481 |
Appl.
No.: |
08/893,856 |
Filed: |
July 11, 1997 |
Related U.S. Patent Documents
|
|
|
|
|
|
|
Application
Number |
Filing Date |
Patent Number |
Issue Date |
|
|
314082 |
Sep 28, 1994 |
5669916 |
|
|
|
Current U.S.
Class: |
606/133; 606/134;
606/43 |
Current CPC
Class: |
A61B
18/203 (20130101); A61K 8/44 (20130101); A61K
8/49 (20130101); A61Q 9/04 (20130101); A61K
8/58 (20130101); A61N 1/30 (20130101); A61K
8/494 (20130101); A61B 2018/00452 (20130101); A61B
2018/00476 (20130101); A61K 2800/434 (20130101); A61K
2800/58 (20130101); A61N 5/062 (20130101) |
Current International
Class: |
A61N
1/30 (20060101); A61B 18/20 (20060101); A61N
5/06 (20060101); A61B 017/50 () |
Field of
Search: |
;606/133,43,134,36 |
References Cited
[Referenced By]
U.S. Patent Documents
Other References
Kennedy J.C. et al., "Photodynamic Therapy with Endogenous
Procoparphyrin IX: Basic Principles and Present Clinical
Experience"; Elsevier Sequoia 6:143-148 (1990..
|
Primary Examiner: Buiz; Michael
Assistant Examiner: Truong; Kevin
Attorney, Agent or Firm: Fish & Richardson P.C.
Government Interests
This invention was made at least in part with funds from the
Federal government under contract N00014-91-C-0084 awarded by the
Department of the Navy. The Government therefore has certain rights
in the invention.
Parent Case Text
This is a continuation of application Ser. No. 08/314,082, filed
Sep. 28, 1994, now U.S. Pat. No. 5,669,916.
Claims
What is claimed is:
1. A method of removing a hair from the skin of a mammal, the
method comprising
(a) applying to the hair a chemical agent that removes the hair
from its follicle, and then
(b) treating the follicle to inhibit its ability to regenerate a
hair.
2. The method of claim 1, wherein the chemical agent breaks
disulfide bonds in the hair.
3. The method of claim 1, wherein step (b) comprises applying a
toxin to the follicle.
4. The method of claim 3, wherein the toxin is an antimetabolic
drug.
5. The method of claim 4, wherein the antimetabolic drug is
5-fluorouracil.
6. The method of claim 3, wherein the toxin is a bleach.
7. The method of claim 4, wherein the bleach comprises a
hypochlorite.
8. The method of claim 4, wherein the bleach comprises a
peroxide.
9. The method of claim 1, wherein step (b) comprises application of
a follicle-inactivating compound and ultrasound waves to the skin,
the ultrasound waves being sufficient to target the
follicle-inactivating compound to the hair follicle.
10. The method of claim 1, wherein step (b) comprises application
of a follicle-inactivating compound and pressure waves to the skin,
the pressure waves being sufficient to target the
follicle-inactivating compound to the hair follicle.
11. The method of claim 1, wherein step (b) comprises application
of a follicle-inactivating compound and heat to the skin, the heat
being sufficient to target the follicle-inactivating compound to
the hair follicle.
12. A method of removing a hair from the skin of a mammal, the
method comprising
(a) mechanically or chemically removing the hair from its follicle,
and then
(b) treating the follicle with a follicle-inactivating
compound.
13. The method of claim 12, wherein step (b) further comprises
application of ultrasound waves to the skin, the ultrasound waves
being sufficient to target the follicle-inactivating compound to
the hair follicle.
14. The method of claim 12, wherein step (b) further comprises
application of pressure waves to the skin, the pressure waves being
sufficient to target the follicle-inactivating compound to the hair
follicle.
15. The method of claim 12, wherein step (b) further comprises
application of heat to the skin, the heat being sufficient to
target the follicle-inactivating compound to the hair follicle.
Description
BACKGROUND OF THE INVENTION
This invention relates to removing hair from skin.
Currently used methods for hair removal include shaving, waxing,
electrolysis, mechanical epilation, chemical depilation, the use of
laser beams (see, e.g., U.S. Pat. Nos. 3,538,919 and 4,388,924),
and the use of light-absorbing substances (see, e.g., U.S. Pat. No.
5,226,907). Some of these methods are painful, inefficient, or time
consuming, and others do have not long-lasting effects.
SUMMARY OF THE INVENTION
I have discovered that mechanical epilation followed by topical
applications causing inactivation of the hair follicle results in
long-term inhibition of hair growth.
Accordingly, the invention features a method of removing a hair
from the skin of a mammal, involving mechanically or chemically
epilating to expose the hair follicle, then treating the follicle
to inhibit its ability to regenerate a hair.
Epilation creates a channel which leads directly and deeply into
the follicle and greatly increases the ability of the follicle to
take up agents which can inactivate the hair growth-promoting
properties of the follicle. Thus, the invention provides an
efficient method for the removal of hair and for long-term
inhibition of hair growth.
In preferred embodiments, epilation is performed using any method
which removes the hair from its follicle, including cold waxing,
warm waxing, and the use of mechanical devices to avulse the hair
from its follicle.
Following epilation, the hair growth-promoting properties of the
follicle are inactivated by any of a plurality of methods,
including the use of photosensitizers followed by exposure to
light, the use of mild toxins, and application of electric current.
Generally, photoinactivation involves (1) application of a
photosensitizer to the skin, (2) uptake of the photosensitizer by
the follicle, and (3) activation of the photosensitizer so that it
inactivates the hair growth-promoting properties of the follicle,
resulting in inhibition of hair growth. Preferably, the
photosensitizer is of low toxicity until it is activated by
exposure to light of a specific wavelength. Preferably, the light
is at a wavelength which is capable of reaching deep into the hair
follicle; generally, a wavelength of 550-800 nm is suitable.
Preferred photosensitizers include, but are not limited to,
porphyrins, phthalocyanines, chlorins, and purpurins. Examples of
suitable photosensitizers are aminolevulinic acid (ALA; activated
at 630 nm), methlyene blue (activated at 660 nm), derivatives of
nile blue-A, porphyrin derivatives such as benzoporphyrin
derivative (BPD; activated at 690 nm), porfimer sodium (e.g.,
PHOTOFRIN.TM. porfimer sodium; activated at 630 nm), purpurins,
chlorins, and phthalocyanines. The photosensitizer can act by
either photochemical or photothermal mechanisms. Photothermal
sensitizers include indocyanine green (activated at 690-800 nm) and
other dyes.
Mild toxins can also be used to inactivate the hair follicle. In
this embodiment, epilation of the hair prior to application of the
toxin results in the targeting of the toxin to the follicle. The
toxin is allowed to interact with the hair follicle for a period of
time sufficient to inactivate the follicle without causing
substantial damage (e.g., ulceration or scarring) to the
surrounding skin; generally, 0.1-5 minutes is a sufficient length
of time. Appropriate toxins include, but are not limited to,
bleaches (e.g., hypochlorites and peroxides), antimetabolic drugs
(e.g., 5-fluorouracil), solvents (e.g., acetone, alcohols, phenol,
and ethers), iodine-releasing agents, detergents and surfactants,
and aldehydes and other protein-crosslinking fixatives (e.g.,
gluteraldehyde, formaldehyde, and acetaldehyde).
In addition, more than one toxin can be used in the invention, with
application of the toxins occurring sequentially or simultaneously
(e.g., a surfactant, a solvent, and an antimetabolic drug can be
combined or used in sequence). One skilled in the art of
dermatology will, with the guidance provided herein, be able to
determine the appropriate conditions required for uptake of the
toxin.
The method of the invention can also employ iontophoretic
techniques to target the follicle-inactivating compound to the hair
follicle. In this embodiment, a solution which includes an ionic
follicle-inactivating compound is applied to the skin following
epilation, and an electric current is then applied to the skin. The
electric current enhances the ability of the follicle-inactivating
compound to penetrate the skin. Useful solutions include, but are
not limited to, hypochlorite bleach, chloride salt solutions, ionic
detergents, and ionic photosensitizers or their precursors (e.g.,
ALA and methylene blue). Appropriate methods and devices for
applying electric current are known in the art (see, e.g.,
Instructions for use by Iomed Inc., Salt Lake City, Utah).
Anesthetics (e.g., lidocaine) can also be iontophoresed in order to
alleviate pain in this embodiment of the invention. A variety of
other methods, including ultrasound or pressure waves, heating,
surfactants, and simple capillary action, can also be used to
target the follicle-inactivating compound to the follicle.
By "epilation" is meant removal of the hair from its follicle.
Epilation can be accomplished by chemical or mechanical means, such
as cold waxing, warm waxing, or grasping the hair and detaching it
to expose the follicle.
By "hair follicle" is meant the downgrowth of the epidermis and the
bulb-like expansion of tissue which houses and creates a hair.
Components of the hair follicle include the external root sheath,
the internal root sheath, the connective tissue papilla, the
matrix, the pluripotential cells which are located approximately 1
mm below the skin surface, and sebaceous glands.
By "inactivation" of the hair follicle is meant inhibition of the
follicle's ability to regenerate a hair and/or the sebaceous glands
which are part of the hair follicle on the face, uppertrunk, and
other body sites prone to acne. Inhibition of hair growth can be
accomplished by destruction of one or more components of the
follicle. The exact target to be destroyed can vary depending on
the composition used to inactivate the hair follicle. Candidate
components to be destroyed include, but are not limited to, the
external root sheath, the internal root sheath, the connective
tissue papilla, the matrix, the sebaceous glands, and the
pluripotential cells which are located approximately 1 mm below the
skin surface.
By "photosensitizer" is meant a compound which, in response to
exposure to a particular fluence, is capable of inactivating a hair
follicle, or a precursor of such a compound which is converted into
a photosensitizer in living cells (e.g., ALA).
By "activation" of a photosensitizer or photosensitizer precursor
is meant exposure of the photosensitizer or precursor to light in
either a pulse or continuous mode, enabling the photosensitizer to
inactivate a hair follicle.
Abbreviations used herein are
ALA: aminolevulinic acid
BPD: benzoporphyrin derivative
PPIX: protoporphyrin IX
Other features and advantages of the invention will be apparent
from the following description of the preferred embodiments
thereof, and from the claims.
DETAILED DESCRIPTION
The drawing will first be described.
Drawing
The Figure is a fluorescence image of PPIX in human skin following
local epilation and application of 20% ALA.
SELECTIVE ABSORPTION BY EPILATED FOLLICLES
Epilation leads to selective uptake of follicle-inactivating
compounds by the exposed follicles.
In the following procedure, epilation was accomplished by cold
waxing a segment of skin of a human subject in order to remove the
hair. Cold waxing is performed by application of a viscous, liquid
wax or resin mixture (e.g., MYEPIL.TM. wax) which, when rapidly
uplifted, avulses each hair from its follicle. As a control, other
sites on the skin were shaved, but not epilated, and all sites on
the skin were then treated as follows. A solution of 20% (wt./wt.)
of the photosensitizer, ALA, was applied to the skin in an
ethanol/water solution, and the treated skin was covered with
plastic wrap for 2-4 hours. ALA is a precursor of protoporphyrin IX
(PPIX), and it is converted into PPIX in living cells. Thus, the
2-4 hour time period is sufficient for uptake of ALA by the
epilated follicle (which occurs within minutes) and conversion of
ALA into PPIX. The absorption of ALA and its conversion to PPIX in
the skin was followed by fluorescence imaging (420 nm excitation;
600+ nm emission). The intense fluorescence shown in the center of
the Figure indicates that cells of the epilated follicles can
convert ALA into PPIX. This image also indicates that epilation
enables the photochemical to selectively penetrate the follicles of
epilated follicles (located at the center of the Figure) as
compared with non-epilated follicles. Thus, epilation facilitates
targeting of the inactivating agent to the follicle.
Inhibition of Hair Growth
Following epilation or shaving (as a control), and application of
ALA, the hair follicles were inactivated by exposing the skin to
varying fluences from 0-300 J/cm.sup.2 of 630 nm (argon-pumped dye
laser) light. At 3 and 6 months after treatment, the number of
regrowing hairs varied from 0% to about 50%. In contrast, 100% of
the hairs on shaven, but not epilated, skin regrew. These data also
indicate that the effectiveness of the method increased with
increasing fluence.
OTHER EMBODIMENTS
Other embodiments are within the following claims. For example, a
mechanical device, instead of waxing, can be used to remove the
hair from the follicle. Chemical agents, e.g., chemical depilatory
cremes which break disulfide bonds in the hair shaft, can be used
as well.
Photosensitizers other than ALA can be used to inactivate the hair
follicle; examples include porphyrins, phthalocyanines, chlorins,
purpurins, and derivatives of rhodamine or nile blue. Indeed, I
have found evidence of selective follicle destruction following
topical application of methylene blue, enhancement of uptake by
iontophoresis, and exposure to light at 660 nm. I also have
detected follicle destruction following application of
chloroaluminum sulforated phthalocyanine and exposure to light at
760 nm. Thus, the usefulness of this invention is not limited to
ALA. Generally, a photosensitizer concentration of 0.1 to 20% is
appropriate; more preferably, the concentration is about 0.5 to 5%;
most preferably, the concentration is about 1%. Several examples of
useful photosensitizers and the appropriate wavelength of light are
provided herein; additional examples will be apparent to those of
skill in the art of photochemistry.
Mild toxins such as bleaches, antimetabolic drugs, solvents,
iodine-releasing agents, detergents, surfactants, and
protein-crosslinking fixatives can be used at concentrations which
inactivate the follicle without causing substantial damage (e.g.,
scarring and ulceration) to the surrounding skin. Generally,
concentrations of 1 to 20% are suitable, with absorption by the
follicle typically lasting 0.1 to 5 minutes.
A variety of dematologically acceptable excipients (e.g., alcoholic
and aqueous solutions, oil-in-water or water-in-oil creams,
emulsions, or ointments) can be used to carry the
follicle-inactivating compound, and acceptable forms of the
excipient include, without limitation, lotions, creams, and
liquids. The vehicle used should carry the photosensitizer or toxin
into the follicle, which is best achieved when a low surface
tension exists between the vehicle and the skin to promote
capillary action. The follicle-inactivating compositions can be
delivered to the follicle by methods other than simple capillary
action, such as those methods which employ ultrasound, heat,
pressure waves, iontophoresis, or surfactants. The amount of time
necessary for uptake of the follicle-inactivating composition will
depend on factors such as the method of application, the properties
of the follicle-inactivating compound, and the excipient which is
used. Generally, the amount of time sufficient for uptake of the
follicle-inactivating compound is 1 to 5 minutes.
Iontophoresis can also be used to facilitate uptake of the
follicle-inactivating compound by the follicle. In skin, the
stratum corneum acts as a barrier to electrical resistance.
Following epilation, the empty follicles are the predominant
pathway by which current flows from an external electrolyte
solution into the skin. Therefore, iontophoresis can enhance the
uptake of ionic follicle-inactivating compounds. In this
embodiment, an electrode of the same polarity as the compound to be
iontophoresed is applied to the skin following application of the
follicle-inactivating compound. (see, instructions for use of
iontophoresis by Iomed Inc., Salt Lake City, Utah). Examples of
ionic follicle-inactivating compounds are ALA, methylene blue,
hypochlorite bleach, chloride salt solutions, and ionic
detergents.
Generally, photosensitizer precursors (e.g., ALA) are converted
into the photosensitizer (e.g., PPIX) within 2-4 hours. The ability
of the photosensitizer precursors to be absorbed by the follicle
and converted into the photosensitizer by cells of the follicle can
readily be assayed by fluorescence imaging as described above. For
improved light coupling into the skin, a layer of mineral oil can
be applied to the skin and covered by a lucite block or other
transparent material which closely matches the skin's refractive
index while activating the photosensitizer with light. The optimal
conditions for hair removal and follicle inactivation can easily be
determined by testing the method on a small segment of the skin and
monitoring the skin for subsequent hair growth.
* * * * *